THE INFLUENCE OF VITAMIN-E QUINONE ON PLATELET STRUCTURE, FUNCTION, AND BIOCHEMISTRY

  • 1 January 1980
    • journal article
    • research article
    • Vol. 55  (6) , 907-914
Abstract
Athough the effects of vitamin E on [human] platelet function have been studied in vivo and in vitro, vitamin E quinone, a natural metabolite of vitamin E, has been overlooked. This oxidized form of vitamin E inhibits platelet aggregation and secretion induced by various aggregating agents more effectively than vitamin E by a magnitude of 5- to 10-fold. Vitamin E and vitamin E quinone do not alter platelet ultrastructure or cellular concentrations of serotonin and adenine nucleotides, including c[cyclic]AMP. Inhibition of aggregation by vitamin E or vitamin E quinone occurs in the absence of detectable reduction of vitamin E quinone or oxidation of vitamin E and is readily reversed by washing the platelets. Only vitamin E quinone prevents arachidonic acid release and slightly inhibits cyclooxygenase, whereas both agents partially prevent Ca release from a platelet subcellular organelle. Vitamin E quinone inhibited synthesis of prostacyclin by endothelial cells with basal synthesis in the presence of external arachidonic acid being less affected than thrombin-stimulated PGI2 production. The greater potency of vitamin E quinone in suppressing platelet function compared to vitamin E suggests that this quinone metabolite may be the better antithrombotic agent and possibly responsible for in vivo effects previously attributed to vitamin E.